Molecular mechanisms underlying the neuroprotection of environmental enrichment in Parkinson's disease.

Parkinson's disease is the most common movement disorder, affecting about 1% of the population over the age of 60 years. Parkinson's disease is characterized clinically by resting tremor, bradykinesia, rigidity and postural instability, as a result of the progressive loss of nigrostriatal dopaminergic neurons. In addition to this neuronal cell loss, Parkinson's disease is characterized by the accumulation of intracellular protein aggregates, Lewy bodies and Lewy neurites, composed primarily of the protein α-synuclein. Although it was first described almost 200 years ago, there are no disease-modifying drugs to treat patients with Parkinson's disease. In addition to conventional therapies, non-pharmacological treatment strategies are under investigation in patients and animal models of neurodegenerative disorders. Among such strategies, environmental enrichment, comprising physical exercise, cognitive stimulus, and social interactions, has been assessed in preclinical models of Parkinson's disease. Environmental enrichment can cause structural and functional changes in the brain and promote neurogenesis and dendritic growth by modifying gene expression, enhancing the expression of neurotrophic factors and modulating neurotransmission. In this review article, we focus on the current knowledge about the molecular mechanisms underlying environmental enrichment neuroprotection in Parkinson's disease, highlighting its influence on the dopaminergic, cholinergic, glutamatergic and GABAergic systems, as well as the involvement of neurotrophic factors. We describe experimental pre-clinical data showing how environmental enrichment can act as a modulator in a neurochemical and behavioral context in different animal models of Parkinson's disease, highlighting the potential of environmental enrichment as an additional strategy in the management and prevention of this complex disease.

Descripción de elementos de radioprotección y dosimetría en unidades de cardiología intervencionista sudamericanas: un estudio piloto / Radioprotection and dosimetry in Interventional cardiology units in South America. a pilot study

ANTECEDENTES: Las unidades de Cardiología intervencional han evidenciado un número creciente de procedimientos, cada vez más variados y complejos, lo cual podría eventualmente generar daños a los profesionales ocupacionalmente expuestos a radiaciones ionizantes (POEs) de no contar con los adecuados elementos de radioprotección y un uso correcto de ellos. OBJETIVO: Caracterizar la disponibilidad y utilización de los elementos de radioprotección y dosimetría de unidades de cardiología intervencionista de centros Sudamericanos. MATERIAL Y MÉTODOS: Se realizó una encuesta autoaplicada a 139 POEs, de ambos sexos de 7 países, a través de una plataforma on-line, se les consultó sobre características demográficas, dosimétricas y de radioprotección. RESULTADOS: Los elementos de radioprotección más tradicionales; delantales y cuellos plomados se utilizaron un 99,5 % y 98,4 % respectivamente, aquellos elementos más recientes como gafas, gorros y paños plomados solo alcanzaron un 36,8 %, 6,8 % y 34,2%, de utilización respectivamente, en cuanto a la utilización de los dosímetros, solo un 7,9 % lo hace apegado a las normas de la Organización Internacional de Energía Atómica (OIEA). CONCLUSIÓN: Se constató en la muestra analizada una falta de elementos de radioprotección y un uso inadecuado de ellos, urge realizar intervenciones educativas y técnicas para mejorar estos datos.

BACKGROUND: Due to the increasing number of interventional cardiology procedures currently performed, health professionals (POE) are exposed to ionizing radiation unless adequate protective elements are used. AIM: to describe the use of radioprotection elements and dosimetry in interventional cardiology laboratories in South America. METHODS: A self-administered survey was performed on 139 POE of both sexes and 7 countries using an online platform. Demographic data, dosimetry and characteristics of radioprotection analyzed. RESULTS: Commonly used radioprotective elements (lead aprons and collars) were used in 99.5% and 98% respectively. Recently introduced protection elements like lead goggles, caps and drapery were used in 36.8, 6.8 and 34.2% , respectively. Dosimetry according to the International Atomic Energy Commission (OIAE) was performed in only 7.9% of the procedures. CONCLUSION: there is a severe lack of adequate radioprotection during interventional cardiology procedures. Urgent measures, including technical implementation and educational interventions are needed to improve radioprotection in interventional cardiology.

Atropine counteracts the depressive-like behaviour elicited by acute exposure to commercial chlorpyrifos in rats.

Acute organophosphate (OP) poisoning induces well-known signs of toxicosis related to acetylcholinesterase (AChE) inhibition. However, the relationship between acute OP poisoning and the onset of psychiatric disorders remains unclear. Thus, we investigated behavioural and biochemical consequences of acute exposure to the OP chlorpyrifos in male rats and also the effectiveness of the antidotes atropine and pralidoxime on reversing these changes. A sub-lethal dose of commercial chlorpyrifos (20 mg/kg, i.p.) elicited signs of acute toxicosis during the first hours after its injection in rats. Twenty-four hours after treatment, this single dose of chlorpyrifos induced a depressive-like behaviour in the rat forced swimming test without impairing locomotor activity. At this time (24 h), chlorpyrifos decreased plasma butyrylcholinesterase (BChE) activity and hippocampal, striatal and prefrontal cortical AChE activity in rats. The behavioural and biochemical consequences of acute chlorpyrifos poisoning do not seem to be long lasting, since 30 days later they were absent. We evaluated whether these behavioural and biochemical consequences of acute chlorpyrifos treatment would be reversed by the antidotes atropine (10 mg/kg i.p.) and/or pralidoxime (40 mg/kg; i.p.) given 1 h after poisoning. Pralidoxime partially reactivated the AChE activity in the prefrontal cortex, but not in the hippocampus and striatum. Atropine attenuated the depressive-like behaviour induced by chlorpyrifos in rats. Our results suggest that acute chlorpyrifos poisoning induces a transient depressive-like behaviour possible related to hippocampal AChE inhibition. They suggest that treatment with atropine and pralidoxime seems to be insufficient to counteract all the effects of OP acute poisoning, at least in rats.

The Environmental Pollutant Tributyltin Chloride Disrupts the Hypothalamic-Pituitary-Adrenal Axis at Different Levels in Female Rats.

Tributyltin chloride (TBT) is an environmental contaminant that is used as a biocide in antifouling paints. TBT has been shown to induce endocrine-disrupting effects. However, studies evaluating the effects of TBT on the hypothalamus-pituitary-adrenal (HPA) axis are especially rare. The current study demonstrates that exposure to TBT is critically responsible for the improper function of the mammalian HPA axis as well as the development of abnormal morphophysiology in the pituitary and adrenal glands. Female rats were treated with TBT, and their HPA axis morphophysiology was assessed. High CRH and low ACTH expression and high plasma corticosterone levels were detected in TBT rats. In addition, TBT leads to an increased in the inducible nitric oxide synthase protein expression in the hypothalamus of TBT rats. Morphophysiological abnormalities, including increases in inflammation, a disrupted cellular redox balance, apoptosis, and collagen deposition in the pituitary and adrenal glands, were observed in TBT rats. Increases in adiposity and peroxisome proliferator-activated receptor-γ protein expression in the adrenal gland were observed in TBT rats. Together, these data provide in vivo evidence that TBT leads to functional dissociation between CRH, ACTH, and costicosterone, which could be associated an inflammation and increased of inducible nitric oxide synthase expression in hypothalamus. Thus, TBT exerts toxic effects at different levels on the HPA axis function.